【Animal Experiment】-The effect of knocking out TRPC6 on MPTP-induced neuroinflammatory injury in mice

  OBJECTIVE: To detect the expression of TRPC6 channel in microglia in a mouse MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-induced neuroinflammation model, and the effect of TRPC6 channel on inflammation The effect of expression was investigated to investigate the effect of damage on dopaminergic neurons.

  Method: In mice injected with MPTP, substantia nigra microglia were classified by magnetic beads labeled CD11b, and TRPC6 expression was detected by Western blotting. After constructing CD11b-TRPC6-/- mice, MPTP-induced microglia proliferation and damage to dopaminergic neurons were detected by immunofluorescence. At the same time, Western blotting was combined with real-time fluorescent quantitative PCR to detect the level of crycB protein and the expression of inflammatory factors after TRPC6 knockout in the MPTP model.

  "Results: In mice injected with MPTP, the expression of TRPC6 channels in microglia was significantly up-regulated. In addition, CD11b-TRPC6-/- mice injected with MPTP had up-regulated cryαB protein levels in microglia. At the same time, MPTP inhibits the proliferation of microglia and the up-regulation of inflammatory factors, reducing the damage to dopaminergic neurons.

  Conclusion: In the MPTP model, the expression of TRPC6 channels in microglia is up-regulated. Knockout of TRPC6 can increase the level of cryαB protein in microglia and reduce the expression of inflammatory factors, thereby reducing the damage to dopaminergic neurons.